These studies in the experimental animal are an extension of previous studies (NIH-NHLI Contract #72-2972-M, 1972-1975) designed to establish the sites, fundamental mechanisms, and stages of ectopic rhythm formation and conduction defects which develop after acute and chronic myocardial ischemia and infarction. The methodology involves integrated studies in the ischemic studies in the ischemic orinfarcte heart in situ and portions of the same heart excised for study by extracellular or intracellular techniques in vitro. Whereas our previous studies have focused on the effects of heart rate and various cardioactive agents on ectopic impulse formation and conduction defects in the acutely ischemic or infarcted heart, the present studies will utilize previously developed and new preparations to investigate the effects of acutely ischemic episodes on the electrophysiologic properties of chronically ischemic hearts; production of accelerated junctional rhythms due to myocardial ischemia; the effects of small vessel ligation (reinfarction) after stabilization of the electrophysiological changes due to large vessel occulsion; and conduction in the His-Purkinje system previously damaged by mechanical trauma which induces scarring. This last study will be an attempt to simulate acute myocardial ischemia occurring in patients with underlying sclero-degenerative disease.